Cardiac pacemakers are medical devices, usually implantable, that provide electrical stimulation in the form of pacing pulses to selected chambers of the heart (i.e., the atrium and/or ventricle). As the term is used herein, a pacemaker is any cardiac rhythm management device that performs cardiac pacing, including implantable cardioverter/defibrillators having a pacing functionality. Pacemakers typically have a programmable electronic controller that causes the pacing pulses to be output in response to lapsed time intervals and sensed electrical activity (i.e., intrinsic heart beats not as a result of a pacing pulse). Implantable pacemakers sense intrinsic cardiac electrical activity by means of internal electrodes disposed near the chamber to be sensed. A depolarization wave associated with an intrinsic contraction of the atria or ventricles that is detected by the pacemaker is referred to as an atrial sense or ventricular sense, respectively. In order to cause such a contraction in the absence of an intrinsic beat, a pacing pulse (either an atrial pace or a ventricular pace) with energy above a certain pacing threshold is delivered to the chamber by an electrode in electrical contact with the myocardium. A wave of depolarizing excitation then propagates through the myocardium, resulting in a heartbeat.
The normal rhythmic impulse of the heart is first generated in pacemaker tissue known as the sino-atrial (SA) node, spreads throughout the atria causing atrial contraction, and is then conducted to the atrioventricular (AV) node where the impulse is delayed before passing into the ventricles. The ventricles of a normal heart are then electrically stimulated by excitation emanating from the AV node that spreads to the heart via specialized conduction pathways known as Purkinje fibers. Coordinated contraction of both atria and both ventricles results in optimally filling of the ventricles with blood before they contract during systole, sometimes referred to as atrio-ventricular synchrony. If either inter-atrial or intra-atrial conduction defects exist, however, the effectiveness of the atria in acting as primer pumps for the ventricles is reduced. Such conduction defects can sometimes result from the stretching of the atrial walls that occurs in patients with congestive heart failure (CHF). It has been found that atrial conduction delays, as reflected by the duration of P-waves on a surface electrocardiogram, are a useful predictor for episodes of paroxysmal atrial fibrillation, where the atria depolarize in a chaotic fashion with no effective pumping action.